Oxidative stress and mitochondrial dysfunction appear early and contribute to the disease progression in Alzheimer’s
disease (AD), which can be detected extensively in AD patients brains as well as in transgenic AD mice brains.
Thus, treatments that result in attenuation of oxidative stress and mitochondrial dysfunction may hold potential for AD
treatment. Geniposide, a pharmacologically active component purified from gardenia fruit, exhibits anti-oxidative, antiinflammatory
and other important therapeutic properties. However, whether geniposide has any protective effect on oxidative
stress and mitochondrial dysfunction in AD transgenic mouse model has not yet been reported. Here, we demonstrate
that intragastric administration of geniposide significantly reduces oxidative stress and mitochondrial dysfunction in
addition to improving learning and memory in APP/PS1 mice. Geniposide exerts protective effects on mitochondrial dysfunction
in APP/PS1 mice through suppressing the mitochondrial oxidative damage and increasing the mitochondrial
membrane potential and activity of cytochrome c oxidase. These studies indicate that geniposide may attenuate memory
deficits through the suppression of mitochondrial oxidative stress. Thus, geniposide may be a potential therapeutic reagent
for halting and preventing AD progress.
Keywords: Alzheimer’s disease, APP/PS1 transgenic mice, cytochrome c oxidase, geniposide, mitochondrial dysfunction, oxidative
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